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Objectives: This systematic review aimed to quantify differences in loneliness levels between autistic and neurotypical samples and investigate the association between loneliness and mental health in autistic individuals. Methods: Three meta-analyses were conducted. Studies were methodologically appraised using established tools. Results: Overall, 39 studies were included. The majority of these achieved moderate methodological quality ratings. The primary meta-analysis (N= 23) found autistic samples reported higher loneliness compared with neurotypical samples (Hedges’ g= .89). The meta-analyses on the associations between loneliness and anxiety (N= 14) and depression (N= 11) in autistic samples found significant pooled correlations (r= .29 and r= .48, respectively). Conclusions: This review highlights numerous limitations within current autism and loneliness research. Nevertheless, loneliness in autism merits targeted clinical and research attention.

Consistent with proposed impairments in the flexible control of action in Obsessive Compulsive Disorder (OCD), previous research has identified a bias towards low-level (action-focussed) rather than high-level (goal-focussed) descriptions of behaviour in individuals with subclinical checking (Belayachi & Van der Linden, 2009).The current study investigated whether this bias could be replicated, or was confounded with the influence of anxiety, and its relationship to another cognitive bias implicated in OCD, namely overestimation of threat. The comparison of high and low checking groups (stratified on anxiety) showed that anxiety was related to a tendency to focus on the mechanics of an action whilst, surprisingly, checking symptoms were associated with a tendency to focus on the goals of an action. These findings suggest that compulsive checkers may habitually attend to “why” actions are performed and their consequences. Additionally, high-level action identification and threat overestimation may provide separable causal influences on OCD.

Our previous neurocognitive studies of schizophrenia outlined two clusters of affected subjects—cognitively spared (CS) and cognitive deficit (CD), the latter's characteristics pointing to developmental origins and impaired synaptic plasticity. Here we investigate the contribution of polymorphisms in major regulators of these processes to susceptibility to schizophrenia and to CD in patients. We examine variation in genes encoding proteins at the gateway of Reelin signaling: ligands RELNand APOE, their common receptors APOER2and VLDLR, and adaptor DAB1. Association analysis with disease outcome and cognitive performance in the Western Australian Family Study of Schizophrenia (WAFSS) was followed by replication analysis in the Australian Schizophrenia Research Bank (ASRB) and in the Health in Men Study (HIMS) of normal aging males. In the WAFSS sample, we observed significant association of APOE, APOER2, VLDLR, and DAB1SNPs with disease outcome in the case–control and CD–control datasets, and with pre‐morbid intelligence and verbal memory in cases. HIMS replication analysis supported rs439401 (APOEregulatory region), and rs2297660 and rs3737983 (APOER2), with an effect on memory performance in normal aging subjects consistent with the findings in schizophrenia cases. APOER2gene expression analysis revealed lower transcript levels in lymphoblastoid cells from cognitively impaired schizophrenia patients of the alternatively spliced exon 19, mediating Reelin signaling and synaptic plasticity in the adult brain. ASRB replication analysis produced marginally significant results, possibly reflecting a recruitment strategy biased toward CS patients. The data suggest a contribution of neurodevelopmental/synaptic plasticity genes to cognitive impairment in schizophrenia. © 2012 Wiley Periodicals, Inc.

Neuritin 1 (NRN1), an activity‐regulated gene with multiple roles in neurodevelopment and synaptic plasticity, is located within the 6p24‐p25 interval on chromosome 6, previously identified as linked to a subtype of schizophrenia (SZ) characterized by pervasive cognitive deficit (CD). We have tested the effect of NRN1sequence variation on susceptibility to SZ and on general cognitive ability in patients and non‐psychiatric control subjects by re‐sequencing the coding regions of NRN1and its flanking sequences, and genotyping 19 single‐nucleotide polymorphisms (SNPs) in 336 SZ patients and 172 healthy control individuals. All participants completed comprehensive neurocognitive assessment, including tests estimating premorbid/prior IQ and current IQ. Logistic regression analyses found no significant association for any of the 19 SNPs with SZ or its CD subtype. However, linear regression analysis gave significant association (P= 0.024 and P= 0.027 after correction for multiple testing) for polymorphisms rs1475157 and rs9405890 with current IQ in the patient group. In SZ, the rs1475157–rs9405890 haplotypes revealed a highly significant association with the abstraction component of current (“fluid”) intelligence (P= 0.0014), and with percentage loss of IQ points between premorbid and current intelligence (P= 0.0041). Results in the control group were not significant after correction. This is the first analysis of association between variation in NRN1and SZ. The findings suggest a role of NRN1as a modifier of cognitive functioning in SZ, with implications for future research into the impact of the environment on the development and maintenance of “fluid” intelligence. © 2009 Wiley‐Liss, Inc.

Memories of conversations are composed of what was said (speech content) and information about the speaker's voice (speaker identity). In the current study, we examined whether patients with schizophrenia would show difficulties integrating speech content and speaker identity in memory, as measured in a gender-identity (male/female) recognition task. Forty-one patients and a comparison group of 20 healthy controls took part in the study. In contrast to controls, patients demonstrated greater impairments in memory for female, but not male, voices. These results are consistent with studies of speech perception that show that female voices have more complex “vocal” characteristics and require greater integration compared with male voices, and with the context memory hypothesis of schizophrenia which suggests that memory binding impairments may result in degraded or incomplete representations of memory traces as the task requirements become increasing complex.

In a previous study we identified a relatively homogeneous subtype of schizophrenia characterized by pervasive cognitive deficit, which was the exclusive contributor to our findings of linkage to 6p25p24. The 6p region contains Dysbindin DTNBP1, considered to be one of the major schizophrenia candidate genes. While multiple studies have reported association between genetic variation in DTNBP1and schizophrenia, the findings have been inconsistent and controversial, leading to recent calls for systematic reexamination and unambiguous evidence of association. To address this, we have undertaken a comprehensive survey of common genetic variation within DTNBP1and its association with schizophrenia, using a HapMapbased genetagging approach. We genotyped 39 tSNPs in a sample of 336 cases and 172 controls of AngloIrish ancestry, with the phenotype defined as clinical schizophrenia, and as composite neurocognitive endophenotypes. Allele and haplotype frequencies, and LD structure in our control sample were similar to those in other European populations. Using multivariate generalized linear modeling, we observed no significant association between any tSNP and any outcome variable. Association with haplotypes was examined across the gene and in the previously associated 5′ region. Neither global haplotype tests, nor specific analysis of the “risk” haplotype previously reported in an ethnically related population, the Irish highdensity schizophrenia families, showed significant evidence of association with schizophrenia or with the neurocognitive endophenotypes in our sample. The framework and results of this study should facilitate further attempts at reanalysis of DTNBP1, in terms of standardized approaches to both phenotype definition and analysis of genetic variation. © 2008 WileyLiss, Inc.

Working memory may be conceptualized as a multi-component system involving the active maintenance and manipulation of stored information in the service of planning/guiding behaviour. Impaired spatial working memory is a robust finding in schizophrenia patients which has been related to an impairment in frontostriatal connectivity. The purpose of this study was to examine the specificity of this impairment by comparing the mnemonic and executive aspects of working memory performance in schizophrenia and bipolar disorder with psychotic features, focusing particularly on the functional dynamics between task components. Twenty-four patients with schizophrenia, 14 patients with bipolar I disorder (manic phase) and 33 healthy control subjects were assessed using the Cambridge Neuropsychological Test Automated Battery (CANTAB): including the spatial working memory (between search errors and strategy scores) spatial span (storage capacity) and spatial planning (Stockings of Cambridge: accuracy and latency) tasks. Both patient groups were impaired on the spatial span task, which requires the maintenance and retrieval of stored information. In contrast, only schizophrenia patients showed a significant deficit in between search errors, which requires both maintenance and manipulation of information in working memory. That is, they exhibited both a mnemonic and an executive dysfunction. Spatial span was particularly important to accurate planning ability in bipolar patients. In contrast, in patients with schizophrenia poor spatial working memory was a significant predictor of planning impairments, consistent with failures in goal selection, evaluation and/or execution. Furthermore, initial planning time was positively correlated with the latency to complete a planning sequence. This pattern of slow cognitive processing in schizophrenia patients only, resembled that reported previously in patients with basal ganglia disorders. These findings are discussed in terms of a possible common disturbance in fronto-parietal circuitry in the two disorders together with a specific disturbance of fronto-striatal circuitry in schizophrenia, that is not present in bipolar disorder.

Accumulating evidence shows that loneliness in psychosis is a major concern for patients, is associated with poorer mental and physical health, and is a significant barrier to recovery. Although psychologists play a major role in treating the cognitive, emotional, and social difficulties of people with psychosis, loneliness is rarely addressed. This article presents a structured review and critique of the evidence base on loneliness in youth and adults with psychosis, framed around the knowledge, attitudes, and skills comprising clinical competencies as a foundation for clinical practice.